Aim: To evaluate thresholds for serum 25(OH)D concentrations in relation to death, kidney progression and hospitalization in non-dialysis chronic kidney disease (CKD) population.
Methods: Four hundred and seventy non-dialysis 3-5 stage CKD patients participating in OSERCE-2 study, a prospective, multicenter, cohort study, were prospectively evaluated and categorized into 3 groups according to 25(OH)D levels at enrollment (less than 20 ng/mL, between 20 and 29 ng/mL, and at or above 30 ng/mL), considering 25(OH)D between 20 and 29 ng/mL as reference group. Association between 25(OH)D levels and death (primary outcome), and time to first hospitalization and renal progression (secondary outcomes) over a 3-year follow-up, were assessed by Kaplan-Meier survival curves and Cox-proportional hazard models. To identify 25(OH)D levels at highest risk for outcomes, receiver operating characteristic (ROC) curves were performed.
Results: Over 29 ± 12 mo of follow-up, 46 (10%) patients dead, 156 (33%) showed kidney progression, and 126 (27%) were hospitalized. After multivariate adjustment, 25(OH)D < 20 ng/mL was an independent predictor of all-cause mortality (HR = 2.33; 95%CI: 1.10-4.91; P = 0.027) and kidney progression (HR = 2.46; 95%CI: 1.63-3.71; P < 0.001), whereas the group with 25(OH)D at or above 30 ng/mL did not have a different hazard for outcomes from the reference group. Hospitalization outcomes were predicted by 25(OH) levels (HR = 0.98; 95%CI: 0.96-1.00; P = 0.027) in the unadjusted Cox proportional hazards model, but not after multivariate adjusting. ROC curves identified 25(OH)D levels at highest risk for death, kidney progression, and hospitalization, at 17.4 ng/mL [area under the curve (AUC) = 0.60; 95%CI: 0.52-0.69; P = 0.027], 18.6 ng/mL (AUC = 0.65; 95%CI: 0.60-0.71; P < 0.001), and 19.0 ng/mL (AUC = 0.56; 95%CI: 0.50-0.62; P = 0.048), respectively.
Conclusion: 25(OH)D < 20 ng/mL was an independent predictor of death and progression in patients with stage 3-5 CKD, with no additional benefits when patients reached the levels at or above 30 ng/mL suggested as optimal by CKD guidelines.
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http://dx.doi.org/10.5527/wjn.v5.i5.471 | DOI Listing |
J Transl Med
January 2025
Medical College of YiChun University, Xuefu Road No 576, Yichun, 336000, Jiangxi, People's Republic of China.
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View Article and Find Full Text PDFNat Cell Biol
January 2025
CNRS UMR144 - UMR3664, Institut Curie, Sorbonne Université, PSL Research University, Paris, France.
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View Article and Find Full Text PDFCurr Drug Targets
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Department of Pharmacology, SVKM's Institute of Pharmacy, Dhule, 424001, India.
Currently, diabetic nephropathy (DN) stands as the predominant global cause of endstage renal disease. Many scientists believe that diabetes will eventually spread to pandemic levels due to the rising prevalence of the disease. While the primary factor leading to diabetic nephropathy is vascular dysfunction induced by hyperglycemia, several other pathological elements, such as fibrosis, inflammation, and oxidative stress, also contribute to the progression of the disease.
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Department of Pediatrics, Texas Children's Hospital, Baylor College of Medicine, Houston, TX, USA.
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View Article and Find Full Text PDFJ Ethnopharmacol
January 2025
Department of Integrative Medicine and Andrology, Zhongda Hospital, School of Medicine, Southeast University, Nanjing 210009, China. Electronic address:
Ethnopharmacological Relevance: Diabetic erectile dysfunction (DED) is a prevalent but often overlooked microvascular complication of type 2 diabetes mellitus (T2DM), with strong associations to cardiovascular disease. The pathophysiology of erectile dysfunction (ED) in T2DM patients is more intricate than in non-diabetic individuals, likely involving multiple pathogenic mechanisms such as endothelial dysfunction, vascular alterations, neuropathy, and oxidative stress. Traditional Chinese Medicine (TCM) has long been utilized in the management of DED, drawing on an extensive body of clinical experience.
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